DISSERTATION ON

A STUDY OF PAROTID SWELLINGS

Submitted to

THE TAMILNADU

DR.M.G.R.MEDICAL UNIVERSITY

in partial fulfillment of the requirement

for the award of degree of

M.S.DEGREE EXAMINATION

BRANCH – I

GENERAL SURGERY

KILPAUK MEDICAL COLLEGE AND HOSPITAL

THE TAMILNADU

DR.M.G.R. MEDICAL UNIVERSITY

CHENNAI

APRIL 2013

CERTIFICATE

This is to certify that “A STUDY ON PAROTID SWELLINGS” is bonafide of

record done by Dr.ANU RAMESH, in the Department of General Surgery, Kilpauk

Medical College and Hospital, Chennai-10 during the post graduate course from 2010-

2013 under the guidance and supervision of Prof.P.N.SHANMUGASUNDARAM,

M.S., in partial fulfillment for the award of M.S. DEGREE EXAMINATION,

BRANCH-I (GENERAL SURGERY) to be held in April 2013 under Tamilnadu Dr

M.G.R. Medical University, Chennai.

Prof. P. N Shanmugasundaram M.S., Dr.P.Ramakrishnan M.D. D.L.O.,

The Professor and HOD, The Dean,

Department of surgery, Kilpauk Medical College

Kilpauk Medical College Chennai-10

Chennai-10

DECLARATION

I declare that this dissertation entitled “A STUDY ON PAROTID

SWELLINGS” is a record of work done by me in Department of General Surgery,

Kilpauk Medical College, Chennai-10 during my Post Graduate course from 2010-2013

under the guidance and able supervision of my unit Chief and Head of Department,

Department of General Surgery Prof.Dr.P.N.SHANMUGASUNDARAM M.S., it is

submitted in partial fulfillment for the award of M.S. DEGREE EXAMINATION-

BRANCH I (GENERAL SURGERY) to be held in April 2010 under the Tamilnadu

Dr.M.G.R. Medical University, Chennai. This record of work has not been submitted

previously by me for the award of any degree or diploma from any other university.

Dr. Anu Ramesh

ACKNOWLEDGEMENT

I whole heartedly thank with gratitude Dr.P.RAMAKRISHNAN M.D. D.L.O.,

Dean, Government Kilpauk Medical College for having permitted me to carry out the

study and to utilize the clinical material in KMCH during the period of my study.

I am greatly indebted to Prof.Dr.P.N.SHANMUGASUNDARAM, M.S.,

Professor & Head of the Department of Surgery, Kilpauk Medical College for having

guided me throughout the period of this work.

I am grateful to Prof.RAJARAMAN, M.Ch, M.S., Professor and H.O.D.,

Department of Surgical Oncology, Government Royapettah Hospital for his immense

help and guidance in carrying out this study.

I thank my Assistant Professors Dr.B.SATHYA PRIYA, M.S.,

Dr.V.KOPPERUNDEVI, M.S., D.G.O. Dr.S.SURESH, M.S., D.A. and

Dr.S.RAJASEKAR, M.S., for their valuable advice, co-operation, guidance,

encouragement and help rendered during the entire period of my study. I sincerely thank

for the help and assistance rendered by my fellow postgraduates. I express my gratitude

to my parents for their help and undying support. Last but not the least; I thank all the

patients for their kind cooperation in carrying out the study successfully.

ABSTRACT

INTRODUCTION:

Swellings of the parotid gland are of special interest to a surgeon’s keen eye.

These lesions are not only involved in diseases isolated to the parotid but can also

present as a part of a generalized systemic disorder, medical or surgical. For a

surgeon the interests lie in the probable origin of the swelling, its involvement of

the facial nerve, the variability in behavior, regarding the operability criteria and its

post-operative complications. A comprehensive knowledge of the anatomy of the

parotid and the prediction of the swelling behaviour can help not only in the

diagnosis but also in ensuring an apt management of the lesion and the patient.

AIMS:

This cohort study was conducted to analyse the following in our institution

1. The incidence of various of parotid swellings.

2. To discuss accuracy of FNAC in comparison to the histo-pathological

reports.

3. The various surgical modalities of treatment of parotid swellings applied .

4. To discuss the post-operative complications.

5. To compare findings of the above study with world statistics.

MATERIALS AND METHODS:

The cohort study which included 45 patients was conducted at Kilpauk

medical college hospital and Government Royapettah Hospital from September

2010 to October 2012. Data was collected from the patients after obtaining an

informed consent. The demographic details of the patients and history of their

swelling was taken. The patients were examined and basic investigations

performed. Details regarding the FNAC report, surgical and non-surgical

management were noted. Post-operative complications were documented. The final

histopathological report was analysed and compared with the FNAC report.

Inclusion criteria were patients with parotid swellings neoplastic and non-

neoplastic and those above 12years of age. Exclusion criteria were patients with

parotid lesions due to systemic or metabolic illness and those with age less than 12

years.

CONCLUSION:

The analysis of the data of the study conducted at our institution provided us

with the following results:

1. Parotid lesions comprised of the most common salivary gland lesions in our

hospital.

2. Amongst the various lesions it was noted that benign tumours were the most

common and the least common were non-neoplastic disorders.

3. The sex incidence showed a similar distribution among both males and females

with the ratio being 1:1.25.

4. The mean age of presentation was 49 yearsand it was seen that the 4th and 7th

decades where the predominant age group for occurrence in case of benign and

malignant tumours respectively.

5. The lesions which were predominant in the non-neoplastic, benign and

malignant tumours groups where abscess, pleomorphic adenoma and

mucoepidermoid carcinomas respectively. These were found to be consistent

with the comparison made with world statistics.

6. FNAC correlated in a total of 39 out of 45 cases, i.e.86.67% of the cases.

The sensitivity and specificity for detection of benign tumors was found to be

93.75% and 100% respectively. In the case of malignant tumours the

sensitivity and specificity was found to be 87.5% and 100% respectively.

7. Patients presenting with facial nerve palsy was seen more amid the malignant

tumors.

8. Most commonly performed surgery was superficial parotidectomy. Completion

parotidectomy was performed in 2 cases and both were malignant tumors with

recurrence.

9. Facial nerve palsy and seroma formation were the commonest complication

noted post-operatively.

10. Radiotherapy was the most common non-surgical modality used and

administered more commonly post-operatively.

CONTENTS

S.NO TITLE PAGE NO.

1. INTRODUCTION 1

2. REVIEW OF LITERATURE 2

3. AIM OF STUDY 57

4. MATERIALS AND METHODS 58

5. OBSERVATION AND ANALYSIS 59

6. DISCUSSION 85

7. CONCLUSIONS 92

BIBILOGRAPHY

APPENDIX

PROFORMA

MASTER CHART

1

INTRODUCTION

Swellings of the parotid gland are of special interest to a surgeon’s

keen eye. These lesions are not only involved in diseases isolated to the

parotid but can also present as a part of a generalized systemic disorder,

medical or surgical. The patient would present invariably due to the

cosmetic problem. For a surgeon the interests lie in the probable origin of

the swelling, its involvement of the facial nerve, the variability in

behavior, regarding the operability criteria and its post-operative

complications. Patients in these cases present themselves to oncologists

and general surgeons alike for the same. A comprehensive knowledge of

the anatomy of the parotid and the prediction of the swelling behaviour

can help not only in the diagnosis but also in ensuring an apt management

of the lesion and the patient.

2

REVIEW OF LITERATURE

"It follows from the complex relations of the parotid that its entire

removal as a surgical procedure is an anatomical impossibility."

Sir Frederick Treves, Surgical anatomist

The parotid gland derives its name from the Greek word meaning

“para auricular” swelling. Surgical treatment of parotid tumors has been

greatly influenced by the intimate relationship of the facial nerve to the

gland. The intricacy of its anatomy to the neuro-vascular structures has

plagued anatomists and surgeons alike for years. McWhorter13

considered

that the gland was divided into two lobes, with an interconnecting

isthmus and the facial nerve passing around the isthmus and between the

two lobes. The consensus has changed over the years to believe that the

gland actually is divided into deep and superficial portions due to the

emergence of the facial nerve. The parotid duct was discovered in 1660

by Niels Stensen and hence named after him1. The first clinical

description of a parotid tumour was given in 1752 by Kaltshmeid,

whereas a classification of tumors was given by Berard in 1841. For

several years the parotid gland surgeries were performed with dismal

results with respect to the facial nerve preservation. In 1892, the first

attempt at total parotidectomy with facial nerve preservation was done by

Codreanu 1. It was Blair in 1912 with careful dissection observing keenly

for facial twitching while stimulating the nerve fibres devised the

3

technique for tumor removal with nerve preservation. But it was Sistrunk

in 1921 who stressed the importance of exposure of the facial nerve while

dissection of the gland1. It has been seen with several studies the

commonest lesions affecting the parotid are the group of benign tumours.

Incidence of non-neoplastic lesions has been found to be rarer in

comparison, varying with studies and inflammatory disorders being the

most common. A R Arshad, et al 16

have seen that the incidence of non-

neoplastic lesions was found to be around 11.8% where as Zbaren et al15

have seen an incidence of 5.7%. Pleomorphic adenoma has been seen to

be the dominant lesion affecting the parotid. The treatment of

pleomorphic adenoma has undergone a vast change from the initially

performed enucleation of the tumour to the present concept of

parotidectomy, superficial or total based on the depth of the tumors.

Malignant parotid tumours are treated based on the lesion, its extent of

involvement and attempts at preserving the facial nerve, unless it is

involved, is the key concept at present. The concept of change to nerve

preservation has brought down morbidity due to the nerve paralysis

significantly improving on the cosmesis and quality of life of patients. An

understanding of the cause-effect relationship of parotid tumours is still

under research though many theories have been proposed regarding them.

4

EMBRYOLOGY:

The development of the parotid gland is mostly seen around the

sixth week of development, as an ectodermal derivative, when the

formation of the duct occurs. It appears as an outgrowth from the oral

epithelium and covers the first branchial arch’s maxillary process. It then

grows posteriorly towards the ear and hence embedding the facial nerve

along with its branches within the substance of the gland. There is then

formation of canals from the solid cords and the differentiation of cells

from the tips leads to formation of acini which are secretory in nature.

Fig. a) DEVELOPMENT OF PAROTID GLAND

5

ANATOMY:

The parotid gland is the largest of the three salivary glands and is

paired. It occupies the parotid region, named so due to the presence of the

gland, which is present from below and front of the ear to below the

zygomatic arch. It has the advantage of an irregular shape hence fitting

snugly in the space provided for it. The gland is divided due to the

presence of the facial nerve in to superficial (endo facial) and deep (exo

facial) parts, around 80% of the gland being superficial. It shares its space

in the compartment with the facial nerve and its branches, external carotid

artery and its terminal branches, retro mandibular (posterior facial) vein

and its divisions, lymph nodes and sensory and autonomic nerves. The

compartment boundaries comprise of the following:

Anterior Border Diagonal line drawn from zygomatic root to the

External auditory canal

Posterior Border External auditory canal

Superior border Zygoma.

Inferior Border Styloid process, styloid process musculature,

internal carotid artery, jugular veins

The superficial part lies over the masseter and mandible, while the

deep part or retro-mandibular portion extends through the

6

stylomandibular tunnel medially, which is in turn formed by posterior

edge of the ramus(ventrally), anterior border of sternocleidomastoid and

posterior belly of digastric (dorsally) and also the stylomandibular

ligament deep dorsally. The stylomandibular ligament in fact separates

the parotid and submandibular glands. The deep part of the gland is seen

in the prestyloid compartment of the Parapharyngeal space and hence

tumors in this portion of the gland can push the tonsillar fossa and soft

palate medially in the intra-oral part. The gland is enclosed within a

capsule continuous with the deep cervical fascia; the layer covering the

superficial surface is dense and closely adherent to the gland forming the

false capsule. A portion of the fascia, attached to the styloid process and

the angle of the mandible, is thickened to form the stylomandibular

ligament. True capsule is formed from condensation of the fibrous stroma

of the gland. The superficial part is somewhat quadrilateral in shape,

being broad above and tapering somewhat below

Five processes have been described in the gland of which three are

said to be superficial while two are deep. The superficial processes are:

1. Condylar 2.Meatal 3. Posterior

The deep processes are

1. Glenoid 2. Stylomandibular

7

Due to the presence of multiple processes it is extremely difficult

to ensure complete clearance of the gland during surgeries and this

difficulty is increased due to the presence of the facial nerve.

The gland has five surfaces, the apex, base or superior surface,

superficial surface, anteromedial and posteromedial surfaces.

The three borders of the gland are anterior, posterior and medial.

Relations of the parotid:

The antero-medial surface is molded on the posterior border of the

ramus of the mandible and clothed by the medial pterygoid and masseter.

The other anterior relations are the lateral surface of the temporo-

mandibiular joint and the emerging branches of the facial nerve.

The postero-medial surface is grooved longitudinally and is seen to

hitch against the external auditory meatus, the mastoid process and

anterior border of sternomastoid. Thus its relations comprise of the

mastoid process with the sternomastoid, posterior belly of digastric,

styloid process and its attachments, external carotid artery which enters

the gland through this surface. The internal carotid artery is deep to the

styloid process in this part.

The superficial surface slightly lobulated is covered by the

integument, the superficial fascia containing the facial branches of the

8

great auricular nerve, platysma muscle and some small lymph glands, and

the parotid fascia which forms the capsule of the gland. Parotid lymph

nodes are embedded within the gland substance.

The superior surface or the base is related to the cartilaginous

portion of the external auditory meatus, temporo-mandibular joint,

superficial temporal vessels and auriculo-temporal nerve. The auriculo-

temporal nerve winds around the neck of the mandible.

The apex of the gland is seen to overlap the posterior belly of

digastric and carotid triangle. Emerging from the apex are the two

divisions of the retro-mandibular veins and the cervical branch of facial

nerve.

The borders of the gland are anterior, posterior and medial. The

anterior border has the following structures emerging from it: the parotid

duct, terminal branches of the facial nerve and transverse facial vessels.

The medial border is present such that it separates the antero-medial and

postero-medial surfaces. The posteromedial and superficial surfaces are

separated by the posterior border.

The process of the gland:

Glenoid process is in the superior part of the gland extends

upwards into the posterior mandibular fossa. The facial process is in the

anterior margin of the gland extending forwards into the masseter.

9

The pterygoid process is seen between the medial pterygoid muscle

and the mandibular ramus.

Intra-glandular structures are( from medial to lateral):

1. External carotid artery and its terminal branches

2. Retromandibular vein

3. Facial nerve and its terminal branches

The external carotid artery lies at first deep to the gland and then

within the gland. In its substance it gives its two terminal branches, the

internal maxillary and the superficial temporal arteries. The former runs

forward deep to the neck of the mandible; the latter runs upward across

the zygomatic arch and gives off its transverse facial branch which

emerges from the front of the gland.

Lateral to the artery the corresponding venous branches internal

maxillary and superficial temporal unite to form the retro-mandibular

vein (posterior facial vein). In the lower part of the gland this vein splits

into anterior and posterior divisions. The anterior division emerges from

the gland and unites with the anterior facial to form the common facial

vein; the posterior unites in the gland with the posterior auricular to form

the external jugular vein.

10

The most superficial of the structures is the facial nerve. The

branches of which emerge from the borders of the gland. The course of

the facial nerve after its exit from the stylomastoid foramen begins with

branches being given off to the stylomastoid, posterior belly of digastric

and posterior auricular muscles before its transition to formation of pes

anserinus which occurs about 1cm anterior and 2 cm below the tragus.

The facial nerve enters the gland from its postero-medial surface. It gives

of its terminal branches from divisions:

1. Temporo-facial – temporal, zygomatic and buccal branches

2. Cervico-facial–marginal mandibular and cervical branches.

The facial nerve and the retro-mandibular vein divide the gland into

superficial and deep parts by the Facio-venous plane of Patey. Several

studies regarding the facial nerve branching pattern have been done and

the following conclusions were made2, 3, 4

.

Type I- No anastomosis occurred between branches of the facial

nerve.

Type II- Presence of an anastomotic connection between branches of

temporo-facial division.

Type III-A single anastomosis between the temporo-facial and

cervico-facial divisions

11

Type IV- Combination of Type II and Type III.

Type V- Two anastomotic rami passed from the cervico-facial

division to intertwine with the branches of temporo-facial division.

Type VI- Plexiform arrangement, the mandibular branch sends a

twig to join any members of the temporo-facial division.

Studies have shown variation in frequency of the type of facial nerve

branching pattern. Weerapant et al2 compared their results with other

groups and found that Type V was the most predominant while Type I

was the least common. Others such as Davis et al3 showed that Type III

was the most common type.

Among the other nerves encountered in relation to the parotid the

greater auricular nerve is the first to be encountered during raising of the

skin flaps and is commonly sacrificed in surgery leading to anaesthesia of

the region. The auriculo-temporal nerve is a branch or the trigeminal

nerve and it relays post ganglionic parasympathetic secreto-motor fibres

to the parotid to from the otic ganglion.

The identification of facial nerve is of critical importance.

The following are the important surgical landmarks for the same5:

1. Tragal pointer- points to the main trunk of VII nerve proximal to

the Pes and is 1–1.5 cm deep and below the pointer.

12

2. Tympano-mastoid suture – when traced medially the main trunk

can be encountered 6–8 mm deep to the suture line.

3. Posterior belly of digastric muscle – It is a guide to the stylo-

mastoid foramen; the trunk of the VII nerve is just superior and

posterior to cephalic margin of the muscle.

4. Styloid process- 5–8 mm deep to the Tympano-mastoid suture;

trunk lies on the postero-lateral aspect of the Styloid near its base

5. By retrograde dissection one of the branches can be traced

proximally

a. Buccal branch- it runs with the parotid duct either superiorly or

inferiorly.

b. Temporal branch- crosses the zygomatic arch parallel with the

superficial temporal artery and vein

c. Marginal Mandibular branch - runs along the inferior border of

the parotid superficial to the retro-mandibular vein.

13

The Stylomastoid foramen is the single most constant landmark.

Fig.b) IDENTIFICATION OF FACIAL NERVE INTRA-

OPERATIVELY WITH LANDMARKS

Fig.c) STRUCTURES RELATED TO PAROTID GLAND (

SECTION TAKEN THROUGH THE GLAND)

14

Fig,d) ANATOMY OF PAROTID GLAND WITH FACIAL NERVE

BRANCHES

15

Stenson’s duct:

It arises from the anterior border of the parotid and parallels the

zygomatic arch, around 1.5cm below the inferior margin. It runs

superficial to the masseter muscle and turns medially 90 degrees to pierce

the buccinator muscle at the level of the second maxillary molar where it

opens onto the oral cavity. It measures approximately 4–6 cm in length

and 5mm in diameter. The buccal branch of the VII nerve runs along with

it.

The Parotid is invested in its own fascia (capsule), which is

continuous with the superficial layer of deep cervical fascia. The Parotid

fascia consists of

1) Superficial layer – extends from the masseter and

Sternomastoid to the Zygoma, and

2) Deep layer – extends from the fascia of the posterior belly of

the Digastric muscle, and forms the Stylomandibular

membrane separating the Parotid and Submandibular glands.

The Parotid fascia sends septa into the glandular tissue, which

prevents the possibility of separating the glandular tissue from its

investing fascia. The attachments of the Parotid fascia include

16

Anteriorly Mandible

Inferiorly Stylomandibular ligament

Posteriorly Styloid process

Vascular supply:

It is supplied by the branches of the external carotid artery and drained by

external jugular vein.

Nerve supply:

It is via the Auriculo-temporal nerve which is a branch of the

mandibular branch of trigeminal nerve.

The parasympathetic nerves are secreto-motor. The preganglionic

fibres begin in the inferior salivary nucleus; pass through the IX nerve, its

tympanic branch, the tympanic plexus and the lesser petrosal nerve and

relay in the otic ganglion. The post ganglionic fibres pass through the

auriculo-temporal nerve and the gland.

Sympathetic nerves are vasomotor and are derived from the plexus

around the external carotid artery.

17

Sensory nerves are from the auriculo-temporal nerve to the gland

but the parotid fascia is innervated by the sensory fibres of the greater

auricular nerve.

Lymph nodes: The parotid nodes lie partly in the superficial fascia

and partly deep to deep fascia over the parotid. This occurs as during

development the parotid is the last to get encapsulated hence results in

encapsulation of the nodes. Also during this process salivary epithelial

cells can be included within the nodes and believed to play a role in

development of Warthin’s tumor5.

HISTOLOGY:

The parotid gland is a predominantly serous salivary gland contains

numerous serous acini. Also there are zymogen granules, intercalated and

striated ducts. Small lymph nodes within the gland give rise to interstitial

lymphocytes. Varying degrees of adipocytes are also seen depending

upon the patient’s age.

The parotid gland secretion is watery and is about 20% of the total

secretion from salivary glands.

18

Fig.e)HISTOLOGY OF PAROTID GLAND

PAROTID LESIONS:

Non-neoplastic disorders of the parotid can be classified as

follows7, 17

:

1. Inflammatory

* Acute (specific)

a. Viral (mumps, Coxsackie virus A, echovirus, and

lymphocytic choriomeningitis)

b. Bacterial (staphylococcal, streptococcal,

pneumococcal, Gram-negative)

Acute suppurative of infancy

Postsurgical

19

Terminal debilitation

* Chronic (specific)

Tuberculosis

Actinomycosis

Sarcoidosis

* 'Recurrent subacute' and chronic recurrent

Self-limited

Progressive

Lymphoepithelial lesion and Sjogren's syndrome

2. Systemic and Secondary Metabolic Disorders

3. Obesity, hypertension, diabetes mellitus, malnutrition and

associated deficiencies (proteins, vitamins), alcoholic liver disease

Hypersensitivity and Drug idiosyncrasy

Local (Salivary Gland) Disturbances

Sialolithiasis

Sialoangiectasis

Trauma, foreign body, fistula

Parotid lymphadenopathy

20

Cysts, mucocele and ranula

Local duct obstructions (mucous plugs, congenital)

4. Miscellaneous

Pneumoparotitis

Psychogenic

Functional over activity

Idiopathic

Irradiation sialadenitis

NON-NEOPLASTIC PAROTID LESIONS :

1. Parotitis :

These are seen to occur due to bacterial, viral causes or as a result

of auto-immune disorders. Viral parotitis is the most common and caused

by paramyxovirus. Other viral infections associated are Epstein-Barr

virus, Coxsackie and parainfluenza virus. Bacterial infections associated

are Staphylococcus aureus and Streptococcus viridans. Bacterial

infections lead to abscess formation. Antibiotics and if necessary incision

and drainage are the mainstay of treatment in the above cases.

Autoimmune disorders such as Sjögren's syndrome, rheumatoid

arthritis and hypergammaglobulinemia. In early part of autoimmune

21

disorders lymphoplasmocytic infiltrate is seen with almost no

parenchymal distortion. If a nodular collection > 50 lymphocytes (“ focus

score”) is seen, the condition is said to be chronic sialadenitis20

. Late in

the disease, near complete absence of acini is noted along with minimal

ducts and dense intra-epithelial lymphocytosis. These conditions can later

on lead to lymphomas.

2. Sialolithiasis

This is seen less in the parotid gland in comparison to the sub-

mandibular gland. They result from the concretions that coalese within

the duct system. It can secondarily lead to chronic sialadenitis. It is a

painful condition associated with increased pain and swelling during meal

times. The stone if radio-opaque can be visualized in radiographs.

Treatment involves removal of the stone and gland portion which is

affected.

3. Chronic Sialadenitis (Chronic Sclerosing Sialadenitis):

It is usually a unilateral condition which occurs most commonly

due to an obstructive sialolithiasis; other causes are radiotherapy or duct

strictures. It is also called Kuttner’s Tumour and can clinically mimic a

neoplasm. Histology will show dilated, secretion filled ducts with

lymphoplasmocytic infiltrate with occasional germinal centre early in the

disease. In late stages, fibrotic ducts surround the gland with acinar

atrophy. Treatment is by surgical excision.

22

Fig.f) HISTOPATHOLOGY OF CHRONIC SIALADENITIS

NEOPLASTIC DISORDERS:

The parotid gland is known for the high preponderance of benign

tumors such as pleomorphic adenoma which is the commonest lesion.

WHO classification of parotid neoplasms.

23

TABLE - 1 WHO CLASSIFICATION OF PAROTID NEOPLASMS

9

MALIGNANT TUMOURS BENIGN TUMORS

Acinic cell carcinoma Pleomorphic adenoma

Mucoepidermoid carcinoma Myoepithelioma Adenoid cystic carcinoma Basal cell adenoma Polymorphous low-grade adenocarcinoma

Warthin tumor

Epithelial-myoepithelial carcinoma Oncocytoma Clear cell carcinoma, not otherwise specified

Canalicular adenoma

Basal cell adenocarcinoma Sebaceous adenoma Sebaceous carcinoma Lymphadenoma- sebaceous and non-

sebaceous Sebaceous lymphadenocarcinoma Ductal papillomas

- Inverted ductal papilloma -Intra ductal papilloma Sialadenoma pappiliferum

Cystadenocarcinoma Cystadenoma

Low-grade cribriform cystadenocarcinoma

Mucinous adenocarcinoma SOFT TISSUE TUMOURS

Oncocytic carcinoma Haemangioma

Salivary duct carcinoma

Adenocarcinoma, not otherwise specified

HAEMATOLYMPHOID TUMOURS

Myoepithelial carcinoma Hodgkin lymphoma

Carcinoma ex pleomorphic adenoma Diffuse large B-cell lymphoma Extranodal marginal zone B-cell lymphoma

Carcinosarcoma

Metastasizing pleomorphic adenoma SECONDARY TUMOURS

Squamous cell carcinoma

Small cell carcinoma Large cell carcinoma

Lymphoepithelial carcinoma

Sialoblastoma

24

The exact etiology of parotid lesions is unknown but several

factors have been implicated including environmental and genetic. Over

time, certain risk factors and clarification of causes have been done

Proof of cause and effect does not exist in any of these postulated

associations, and the etiology of most salivary gland cancers cannot be

determined

ETIOLOGY OF NEOPLASTIC LESIONS:

J.W. Eveson et al9 study on neoplastic lesions proposed the

following causes.

1. VIRUSES:

Strong associations between lympho-epithelial carcinomas and

Epstein - Barr virus (EBV) have been made9.

2. RADIATION:

Evidence to understand compelling links between ionizing

radiation and parotid tumors have been studied. Follow-up on a long term

basis of atomic bomb victims showed contributory evidence towards an

increase in these tumors. Those undergoing therapeutic radiation for the

head and neck tumors also have an increased risk.

25

3. OCCUPATION:

Industrial workers such as those in rubber manufacturing and

plumbing industry due to exposure to metal and nickel compounds are

prone for parotid tumors. Also those individuals in the woodworking,

automobile industries and employed in asbestos mining are prone for

increased risk of parotid tumors.

4. LIFE STYLE :

Though no association has been found between alcohol

consumption, a definite association is found between Warthin’s tumor

and smoking. An increased level of risk has also been postulated in those

with high cholesterol intake.

5. HORMONES:

Conflicting reports regarding associations of endogenous hormones

in parotid tumors have been reported. Estrogen receptors were found in

nearly 80% of normal glands in males and females. Estrogen receptors

have been reported in a minority of cases of acinic cell carcinoma,

mucoepidermoid carcinoma and salivary duct carcinoma, but not detected

in adenoid cystic carcinoma9. Certain studies have also reported estrogen

receptors in pleomorphic adenoma.

26

Progesterone receptors are noted with high levels of expression in

recurrent pleomorphic adenoma. Among malignant lesion, they were seen

acinic cell carcinoma, adenoid cystic carcinomas and mucoepidermoid

carcinomas.

Androgen receptors are present in 90% of salivary duct

carcinomas. A recent study has also shown this immune-reactivity in

carcinoma ex pleomorphic adenoma and basal cell adenocarcinoma and a

fifth of cases in the study showed positivity in acinic cell carcinoma,

mucoepidermoid carcinoma and adenoid cystic carcinoma.

PAROTID TUMORS:

BENIGN TUMORS:

1. Pleomorphic Adenoma-

It is also known as benign mixed tumor as originally said by

Minssen in 1874 and comprises of multiple histologic components

including myxoid, mucoid, chondroid and other elements, hence known

for its heterogeneity. These comprise almost 80% of parotid neoplasms9.

To distinguish from a malignant transformation, features such as cellular

atypia, mitosis, perivascular and perineural invasion are relied upon.

They are slow growing, painless tumors, arising in 90% of cases from the

superficial lobe. These tumors are noted to have pseudopods and hence

have a tendency to recur if only enucleated.

27

The epithelial component consists of ductal structures with an

associated myoepithelial layer, but also may contain collections of

myoepithelial cells that may be spindled, clear, plasmacytoid, or basaloid.

The mesenchymal, or stromal, component is typically myxoid, hyaline, or

chondroid

Pleomorphic adenomas have been divided into a myxoid type

(>80% mesenchymal-type tissue), cellular type (>80% epithelial-type

tissue), and mixed or classic type (generally an equal mix of

components)20

. Treatment is surgical and superficial parotidectomy is

done in most cases. Total parotidectomy is done for deep lobe

involvement.

Fig.g) MICROSCOPIC PICTURE OF PLEOMORPHIC

ADENOMA

28

2. Warthin’s tumor:

This is also known as papillary cystadenoma lymphomatosum. It is

the second most common benign parotid neoplasm associated with a10%

bilateral incidence, male predominance and multi-centricity. Also it is

almost exclusively found in the parotid gland. As mentioned earlier the

late encapsulation of the gland and lymphatic tissue trapping during

development favours the formation this tumor. Another salient feature of

this tumor is that it contains plenty of mitochondrial rich oncocytes and

hence presents as hot spots on radio nucleotide with Technetium 99M21

.

Microscopically what we see characteristically are two-tiered epithelial

layer, lining the branching, cystic or cleft-like spaces and immediately

subjacent, well-developed lymphoid tissue sometimes forming germinal

centers20

.

Fig. h)MICROSCOPIC PICTURE OF WARTHIN'S TUMOUR

29

3. Basal cell adenoma:

They are benign tumors basaloid cells. They tend to occur

generally in adults with 75% occurring in the parotid gland. They are

usually asymptomatic, slow growing lesions. A subtype called the dermal

anlage tumor may be multicentric and may be associated with various

adenexal skin tumors. Though four patterns are seen microscopically, the

tumor is composed of 2 cell types. Small cells with little cytoplasm

typically lie at the neoplasm's edge, frequently show peripheral

palisading, and give the tumor its basaloid appearance. The other type

being more polygonal basaloid cells with slightly more cytoplasm and

round to oval nuclei containing more open chromatin usually lay in the

tumor's center. They are immunopositive for pan-cytokeratin S-100,

smooth muscle actin, and muscle-specific actin, all evidencing

myoepithelial differentiation.

4. Myoepithelioma :

These are benign tumors which are almost exclusively composed

of myoepithelial cells although a small percentage can be made up of

ductal cells. Hence they are considered to lie at one of the spectrum with

basal cell adenoma at the opposite end and pleomorphic adenoma more in

the center20

. It is seen to occur in almost equal frequency in the parotid

gland and minor salivary glands. Histologically the lesion comprises of

30

sheets and cords of tumor cells. They are classified into four sub-types all

of which have collagenous or myxoid stroma:

I) Spindle-cell II) Hyaline III) Plasmatoid

IV) Clear cell

Cells stain strongly positive for S-100 and cytokeratin and are

variably reactive to smooth muscle actin and glial fibrillary acid protein

(GFAP)20

.

MALIGNANT TUMORS:

1. Mucoepidermoid carcinoma:

It is the most common parotid malignancy, composed of mucous,

intermediate, and epidermoid (or squamoid) cells. They are noted to be

slightly more common in women with a mean incidence around the 5th

decade of life20

. Patients present with a slow growing, painless mass.

Hallmark of these tumors is the presence of three different cell types

which can occur in sheets, nests, duct like structures or cysts. Frequently

intermediate cells predominate, ranging from small basal cells with

minimal basophilic cytoplasm to larger oval cells with pale eosinophilic

cytoplasm. The mucin-producing cells are organized singly or in clusters ,

with pale, foamy cytoplasm, distinct cell membranes, and eccentric small

nuclei. They line cystic spaces and are positive with mucicarmine or PAS

stains20

. Abundant eosinophilic cytoplasm and vesicular nuclei are seen in

epidermoid or squamoid cells. Immunohistochemistry is of little utility in

31

the diagnosis of mucoepidermoid carcinoma. Many mucoepidermoid

carcinomas possess a t (11;19)(q21;p13) translocation20

. Tumors that

carry the rearrangement are associated with a better clinical outcome.

Prognosis is highly dependent on the grade of the tumor. Low-grade

lesions are markedly cystic, and have abundant well-differentiated

mucous cells. High-grade lesions are more solid with squamous and

intermediate cells predominating.

Table - 2

BRANDWEIN GRADING OF MUCOEPIDERMOID

CARCINOMA20

:

PARAMETER POINTS

Cystic component<25% 2

Tumor front invades in small

Nests and islands 2

Pronounced nuclear atypia 2

Lymphatic and or vascular invasion 3

Neural invasion 3

Necrosis 3

4+ mitosis/ 10 HPF 3

Bony invasion 3

32

Table - 3

GRADING OF MUCOEPIDERMOID CARCINOMA

Grade Point score/mortality (%)

Low (I) 0

Intermediate (II) 2–3

High (III) 4 or more

Wide local resection has to be done for these tumors. Radiation can

be used in cases of recurrence or for palliation in case of unresectable

lesions. Prognosis depends upon the grade of the tumor, excellent for low

grade (>90%) and poorer for high grade tumor (about 50%)20

.

Fig.i) MICROSCOPY OF MUCOEPIDERMOID TUMORS

33

2. ACINIC CELL CARCINOMA:

It accounts for a total of 1%–3% of salivary gland tumors of which

it’s most common location is the parotid. It is the second most common

malignancy20

. It presents as a slowly growing mass, can be occasionally

painful. It is seen usually as a single, circumscribed, solid mass and can

undergo cystic degeneration. Histological variability is seen. It can be

solid or lobular, microcystic, papillary-cystic or follicular. Small tumors

due to their well-differentiated state can be missed easily. The

characteristic cell seen is the acinic cell, which has the appearance of a

salivary acinar cell with abundant granular, basophilic cytoplasm and a

small, round, eccentrically placed nucleus. With PAS staining

cytoplasmic zymogen granules are seen. A mixture of architectural

patterns is seen and characteristic dense lymphoid infiltrate is also seen.

Due to lack of tumor infiltration at the tumor periphery it can be confused

as benign. Differential diagnosis includes a normal parotid gland,

oncocytoma, clear cell carcinoma, cystadenocarcinoma. Adequate

resection is necessary as recurrence is seen in about one- third of cases. It

is considered as a low-grade malignancy, but around 10%–15%

metastasizes regionally to lymph nodes or in a distance to lungs and

bones. Survival rate is around 80% in 5 years20

.

34

Fig.j) MICROSCOPIY OF ACINIC CELL CARCINOMA

3. ADENOID CYSTIC CARCINOMA:

Peak incidence of this tumour is seen in patients between 40 and 60

years of age. It is slow growing and progressive in nature. Perineural

invasion is characteristic to this disease and at times it can be the

presenting symptom of the disease such as facial nerve palsy. Varying

architectural patterns can be seen, cribriform, tubular, solid and mixed.

Grading is based on the dominant pattern; most commonly seen is

cribriform, consisting of cell nests arranged around gland-like spaces

filled with PAS positive granular basophilic material. The spaces are

actually extra-cellular cavities containing reduplicated basal lamina and

myxoid material. The tumor cells are basaloid with round to oval,

hyperchromatic nuclei without nucleoli and very little cytoplasm.

35

Grading of Adenoid Cystic Carcinoma

Predominant pattern Grade

Tubular I

Cribriform II

Solid III

Perineural invasion is common in the tumor periphery.

Immunohistochemistry is of little use. Positive reaction for cytokeratins,

collagen type IV and laminin and partial reactivity towards myoepithelial

markers is seen. This tumor is highly malignant and progressive.

Compared to other cancers this has a lower survival rate of around 62% at

five years20

. Involvement of bone, perineural invasion and solid type of

tumors show poorer prognosis.

Fig.k) MICROSCOPIC PICTURE OF ADENOID CYSTIC

CARCINOMA

36

4. MALIGNANT MIXED TUMORS:

This term is broadly used to true malignant mixed tumors,

carcinoma ex pleomorphic adenoma and metastatic mixed tumor20

.

I) True salivary gland mixed tumor( carcinosarcoma)

This is composed of both carcinomatous and sarcomatous

components and is extremely rare, About one third of patients have pre-

existing pleomorphic adenoma. It presents around the sixth decade and

microscopically it is seen to have an intimate admixture of both

components. High grade duct carcinoma or undifferentiated carcinoma

mixed with fibrosarcoma, leiomyosarcoma or liposarcoma is seen20

.

These are extremely aggressive tumors treated with wide local excision n

and radiotherapy.

II) Carcinoma ex pleomorphic adenoma:

These account for >95% of mixed malignant tumors. The classical

history is a long standing parotid mass that has undergone rapid growth

over few months. The risk of malignancy increases with the number of

years the tumour is left untreated, 1.5% in 5 years and 9.5% in 10 years21

.

The proportions of carcinoma and pleomorphic adenoma can vary; the

malignant component can be poorly differentiated adenocarcinoma,

salivary ductal carcinoma or undifferentiated carcinoma. Prognosis is

dependent upon the carcinoma type and extent of invasion. Invasion is

37

classified as intracapsular (noninvasive), minimally invasive (≤ 1.5mm in

the greatest extent) or invasive (≥1.5mm in the greatest extent) 20

. Wide

resection with lymph node dissection in cases of nodal metastasis is done

and radiotherapy provided postoperatively or for invasive and inoperable

tumours.

III) Metastasizing mixed tumor:

This is the least common. Histologically they resemble

pleomorphic adenoma but are associated with metastasis to local lymph

nodes or distant organ metastasis.

5. SALIVARY DUCT CARCINOMA:

This is one of the most aggressive primary salivary gland tumors.

This resembles high-grade ductal carcinoma of breast. Male are more

commonly affected and clinically it seen as a rapidly growing parotid

mass with skin and facial nerve involvement. These are well demarcated

and partly encapsulated with invasion into adjacent parenchyma.

Microscopy shows ductal structures lined by eosinophilic cells with

supporting layer of clear myoepithelial cells with hyalinized, eosinophilic

stroma between cells. Wide local excision and radiotherapy are the

treatment modalities.

38

6. LYMPHOMA:

It is extremely rare and can occur in < 5% of patients with parotid

lesions. Suggestive clinical features are development of a parotid mass in

a known patient of malignant lymphoma, or suffering from an immune

disorder (Sjogren’s syndrome, rheumatoid arthritis or AIDS) or in an

individual with a previous benign lymphoepithelial lesion. The prognosis

is usually better than nodal lymphoma of same histology.

A

B

Fig. l) LYMPHOMA OF PAROTID GLAND -A. MICROSCOPIC

PICTURE B. CT PICTURE

39

7. METASTASIS TO PAROTID:

As such the metastasis is more to the intra or periglandular lymph

nodes and they are most commonly from the primary tumors of the head

and neck. The parotid nodes provide the drainage basin from the scalp,

face, ear skin, external auditory canal and tympanic membrane. Hence

squamous cell carcinomas and melanomas account for around 80%. The

remainder is most commonly from the lung, kidney and breast

carcinomas.

PHYSICAL EXAMINATION:

The diagnosis depends upon essential findings in the history and

physical examination. In the examination one should focus on the extent

of disease in the parotid, neck, local effects of the lesion and nerve

involvement. The mass is palpated to determine presence of pain, its

consistency, mobility and fixity to the adjacent tissue. The skin of scalp,

face and ear is examined for lesions. Any evidence of neck node

involvement is palpated for. Oral cavity is examined for the duct opening

and deep lobe assessment. The pharyngeal wall is examined for deviation

and jaw is examined for trismus. Findings suggestive of malignancy

include a large, fixed mass, facial nerve weakness, nodal metastasis, skin

involvement and at times trismus.

40

Fig.m) PAROTID GLAND TUMOUR

Fig.n) PAROTID LESION SEEN IN THE TAIL REGION

41

STAGING OF PAROTID TUMORS

TNM staging

PRIMARY TUMOUR:

TX Primary tumor cannot be assessed

T0 No evidence of primary tumor

T1 Tumor ≤2 cm in greatest dimension without extra parenchymal

extension

T2 Tumor >2 cm but not >4 cm in greatest dimension without extra

parenchymal extension

T3 Tumor >4 cm and/or tumor having extra parenchymal extension

T4a Tumor invades skin, mandible, ear canal, and/or facial nerve

T4b Tumor invades skull base and/or pterygoid plates and/or

encases carotid artery

REGIONAL LYMPH NODES (N)

NX Regional lymph nodes cannot be assessed

N0 No regional lymph node metastasis

N1 Metastasis in a single ipsilateral lymph node, ≤3 cm in greatest

dimension

42

N2a Metastasis in a single ipsilateral lymph node, >3 cm but not >6

cm in greatest dimension

N2b Metastasis in multiple ipsilateral lymph nodes, none more than

6 cm in greatest dimension

N2c Metastasis in bilateral or contralateral lymph nodes, none >6 cm

in greatest dimension

N3 Metastasis in a lymph node, >6 cm in greatest dimension

DISTANT METASTASIS (M)

MX Distant metastasis cannot be assessed

M0 No distant metastasis

M1 Distant metastasis

Table 4: STAGE GROUPING- AJCC

STAGE GROUPING

Stage I T1 N0 M0

Stage II T2 N0 M0

Stage III T3 N0 M0

Stage III T1 N1 M0

Stage III T2 N1 M0

43

Stage III T3 N1 M0

Stage IVA T4a N0 M0

Stage IVA T4a N1 M0

Stage IVA T1 N2 M0

Stage IVA T2 N2 M0

Stage IVA T3 N2 M0

Stage IVA T4a N2 M0

Stage IVB T4b Any N M0

Stage IVB Any T N3 M0

Stage IVC Any T Any N M1

PROGNOSTIC FACTORS:

1. Age at diagnosis 2. Pain at presentation 3. T stage

4. N stage 5. Skin invasion 6. Facial nerve dysfunction

7. Perineural growth 8. Positive surgical margins

9. Soft tissue invasion 10. Treatment type

44

MANAGEMENT

INVESTIGATIONS:

FINE NEEDLE ASPIRATION:

Cytological analysis which can be achieved through FNA is helpful

in a pre-operative evaluation to distinguish between malignant and benign

lesions. It is considered safe when done with 23 gauge needle. It can also

be done with a 25 gauge needle11.

Most commonly performed blindly in the outpatient clinic and has

several advantages – it is quick, safe and accurate in the hands of a skilled

practitioner and high levels of diagnostic accuracy. Accuracy increases

when used under ultrasound guidance12

. An average accuracy is estimated

around 54% to98%. The diagnostic accuracy is less in cases of malignant

lesions compared to benign ones. Sensitivity up to 70% and specificity

around 94% can be obtained. It can be useful to distinguish not only

between benign and malignant tumor, but also salivary and non-salivary

processes. It can be indicated to identify suspected malignancies,

diagnose metastatic carcinomas, suspected lymphomas and evaluate

bilateral tumors. Also it helps enable conservative management in

Warthin’s tumour or pleomorphic adenomas in poor risk patients. A study

by A.M. Contucci et al26

where the FNA and final histopathology were

compared showed sensitivity and specificity of 57.3% and 100%

respectively with and overall diagnostic accuracy of 94%.

45

RADIOLOGICAL INVESTIGATIONS:

1. SIALOGRAPHY:

This helps in diagnosing lesions of the Stenson’s duct such as

strictures, calculi. Also in the presence of any parotid enlargement the

displacement of the duct can be seen. It is rarely used, both because there

is a significant possibility of an infectious flare-up and because the study

actually yields only minimal information.

2. ULTRASOUND;

It helps to distinguish between solid and cystic lesions and also to

identify lymph nodes. An important application is when it is used in

guided FNAC increases the accuracy of FNAC.

Fig.o) ULTRASOUND OF PAROTID LESION- CYSTIC

APPEARANCE

46

A study published regarding ultrasound guided FNA showed that in

74 out of 76 cases a cytological diagnosis was achieved22

.

3. CT

CT is superior to MRI for evaluation of the bony structures. It is

indicated in patients with diffuse enlargement of the parotid gland, tumor

extension beyond the superficial lobe, facial nerve weakness, trismus, or

deep-lobe parotid tumors that are difficult to evaluate clinically10

. If the

parotid mass appears to be fixed to the deeper structures, it is appropriate

to proceed with CT to evaluate the extent and parapharyngeal extension

of the disease.

Fig.p)CT PICTURE OF PAROTID NEOPLASM

47

Fig.q)CT PICTURE OF ACUTE PAROTITIS

MRI:

MRI helps to distinguish inflammatory lesions from neoplasms of

the parotid. It is indicated in cases of facial nerve palsy. It also is helpful

in distinguishing deep lobe tumors from other parapharyngeal masses,

evaluating suspicious lymph nodes and the periphery of the mass

RADIONUCLEOTIDE TECHNITIUM 99M SCAN:

This is seen to be helpful in identifying Warthin’s tumors and

oncocytomas as hot spots that they present with due to the presence of

oncocytes. They are not used presently as before.

48

Fig.r) RADIONUCLEOTIDE SCAN IN ONCOCYTOMA

TREATMENT:

Surgery is the primary treatment done for most of the parotid

swelling presenting in a Surgical department. Other modalities which

may be used are radiotherapy as an adjuvant or neo-adjuvant form.

Chemotherapy is administered in cases of palliation or lymphomas.

SURGICAL:

Principles of treatment of parotid lesion10

:

1. Adequate local excision of tumor, based on extent of

primary lesion and the primary lesion itself.

2. Preservation of facial nerve if possible

3. Elective neck dissection reserved for selected patients

49

4. 4.Postoperative radiotherapy when indicated (in appropriate

fields)

5. Prognosis determined primarily by stage and grade of tumor.

The basic types of surgeries done for removal of the parotid gland

are as follows:

1. Superficial parotidectomy

2. Total conservative parotidectomy

3. Radical parotidectomy

1. SUPERFICIAL PAROTIDECTOMY:

It is the minimal surgical procedure for a parotid mass requiring

removal involving the superficial lobe. Identification and dissection of the

facial nerve is of extreme importance as otherwise inadvertent injury can

occur. General anaesthesia without muscle relaxation should be

advocated for this. Incision for the procedure should be planned keeping

the adequate surgical exposure and cosmesis in mind. It begins anterior to

the ear, just above the tragus, continuing downward past the tragus,

curving behind the ear and turning downward to descend along the

sternocleidomastoid. The incision is deepened upto the subcutaneous

level and a plane is developed between the external ear canal and the

posterior aspect of the parotid. Anterior flap is created in a plane

superficial to the parotid fascia. The sternomastoid muscle after

50

identifying its anterior border is retracted after dissecting the gland from

it. The Greater auricular nerve may be sacrificed if required. Dissection

should be continued along the plane and attachments to the mastoid be

cut and the posterior belly of digastric muscle is identified. Dissection

should be done in a vertical plane to minimize risk of injury to the distal

branches of facial nerve10

. At this point the identification of the facial

nerve should be made as it emerges from the stylomastoid foramen. The

nerve can be identifies by an antegrade or a retrograde approach. In the

antegrade approach the main trunk of the nerve is identified, usually

located at a point which underlies the halfway point between mastoid

process tip and ear canal. Other landmarks include tragal pointer, the

posterior digastric belly and tympanomastoid suture. To ensure the safety

of the nerve, several centimeters of the parotid need to be mobilized. At a

proximity to the nerve electrocautery is best avoided. Retrograde

approach is used when the main trunk cannot be exposed and hence

dissection is proceeded from a peripheral branch to the main trunk.

Alternatively nerve stimulator may be used to identify the branches. Once

the nerve trunk has been identified and dissected all around carefully,

sharp dissection is used to divide the gland substance while protecting the

nerve. It is important that each division of the gland reveals more of the

nerve. Once the dissection is done, all the branches of the nerve have

been defined and the superficial part of the gland removed, after ensuring

hemostasis the wound can be closed with a suction drain in situ. The

patient is closely monitored for any facial nerve palsy.

51

2. TOTAL PAROTIDECTOMY

This is employed in case of malignant lesions and lesions with

deep lobe involvement. After proceeding as superficial parotidectomy the

nerve trunks are gently retracted and excision of the deep lobe is done. In

case there is retromandibular extension of the tumor, the incision can be

extended anteriorly over the mentum and paramedian mandibulotomy can

be performed.

Fig. s) SPECIMEN OF TOTAL PAROTIDECTOMY

3. RADICAL PAROTIDECTOMY:

It is employed for patients with advanced parotid carcinomas.

Facial nerve is sacrificed. Extended radical surgery involves resection of

overlying skin, adjacent mandible and soft tissue, temporal bone and

portion of the adjacent external ear. Free tissue transfer used for repair of

facial nerve.

52

Fig.t) INTRA-OPERATIVE FACIAL NERVE IDENTIFICATION

Fig. u) SPECIMEN OF EXTENDED RADICAL

PAROTIDECTOMY

53

4. NECK DISSECTION:

In patients which detectable neck nodes, high grade tumors and

infiltrative tumors it is commonly performed. The decision to employ a

radical, modified radical or functional neck dissection is made based on

the grade of tumor and nodal involvement.

SURGICAL COMPLICATIONS:

Complications which occur due to parotidectomy are related to the

meticulous dissection, the lesion and anatomy identification. The most

commonly seen complication is facial nerve involvement, which could be

temporary or permanent. Other complications such as Frey’s syndrome

though inferred from previous studies found to be common, it is now seen

that the incidence is actually much less than expected. A study18

classified the complications based on the time of occurrence, into intra-

operative, early and late complications. The following possible

complications can be seen:

1. Facial nerve palsy: It may be transient of permanent. If the nerve

transection is identified intra-operatively primary repair may be done

either as a tension free anastomosis or interposition nerve grafts. An

incidence ranging from 17% to 100% can occur as transient facial nerve

paralysis depending upon the extent of resection and tumour location. 10

.

Permanent paralysis has been seen fortunately in less than 5% of cases. 10

.

54

2. Gustatory sweating (Frey’s syndrome) : It occurs when there is

cross-innervation of parasympathetic and sympathetic fibres which

supply the parotid. On chewing food there is sweating, flushing and skin

warmth. Symptomatic treatment alone is adequate in a majority of

patients. Though there it has been extensively been written about, its

general incidence is low, but varies with centres. Some have reported as

high as 50%18

. Conservative management is usually advocated with

application of topical anti-perspirants but surgeries such as superficial

temporal artery fascial flap positioning are also done in severe cases.

Newer modalities to treat this condition include botulinum toxin (BTX)

injection.

3. Salivary fistula: Also called sialocele it is usually self-limiting

condition seen in 1%–15 % of parotidectomies10

. Its attributed more to

gland disruption than injury to Stenson’s duct. Conservative management

with anti-cholinergics may be done, other than which at times completion

parotidectomy and low dose radiation may be employed. Staffieri et al.

first proposed, in 1999, BTX in the treatment of salivary fistula and

sialoceles after conservative treatment failure 19

.

4. Seroma

5. Flap necrosis- it has been noted to occur at the distal tip of the

posterior auricular flap.

55

6. Keloid formation

7. Cosmetic deformity

8. Hemorrhage

9. Wound infection

10. Hypoaesthesia over Greater auricular nerve distribution

Fig.v) FLAP NECROSIS SEEN ON 6TH POST-OPERATIVE DAY

RADIOTHERAPY:

Indications:

1. Highly malignant, aggressive tumor

2. Invasion of tissues adjacent to parotid capsule

3. Regional lymph nodal metastasis

4. Deep lobe cancers

56

5. Recurrent tumors

6. Facial nerve infiltration by tumor.

The minimal treatment volumes for the parotid lesions are the

parotid bed and upper neck nodes. Tumour dose to the primary area is

around 60 to 65 Gy in a period over 7 weeks. Higher dosage is used for

microscopic positive margins or gross disease.

Complications:

1. Xerostomia 2. Tismus 3. Otitis media 4. Osteoradionecrosis

5.hair loss

CHEMOTHERAPY:

Cisplatin, paclitaxel, vinorelbine, epirubicin and mitoxantrone have

had good response in around 10%–20% of studies. But response is still

limited and several trials are ongoing. Trials are also underway for

targeted therapy.

57

AIM OF THE STUDY

1. To study the incidence of various of parotid swellings in our

institution.

2. To discuss accuracy of FNAC in comparison to the histo-

pathological reports in our institution.

3. To study the various surgical modalities of treatment of

parotid swellings applied in our institution.

4. To discuss the post-operative complications in our

institution.

5. To compare findings of the above study with world statistics.

58

MATERIALS AND METHODS

The cohort study which included 45 patients was conducted at

Kilpauk medical college hospital and Government Royapettah Hospital

from September 2010 to October 2012. Data was collected from the

patients after obtaining an informed consent. The study group consisted

of 19 males and 26 female patients . The age group ranged from 16 years

to 77 years. FNAC was performed in all patients. A total of 7 non-

neoplastic, 22 neoplastic and 16 malignant lesions were identified. Forty

one patients were operated on and histopathology of specimens was done

in 41 cases, which included 4 cases where only biopsy was performed.

Postoperative radiotherapy was given in 10 cases while palliative

radiotherapy was provided in 4 cases. One case underwent chemotherapy.

Inclusion criteria :

Patients with parotid swellings neoplastic and non-neoplastic

Age of 12years and above.

Exclusion criteria:

Patients with parotid lesions due to systemic or metabolic illness.

Age less than 12 years

59

OBSERVATION AND ANALYSIS

The observation of the study of 45 parotid lesions yielded the

following results:

1. OVERALL INCIDENCE

LESION TOTAL NUMBER

OF CASES

PERCENTAGE

Non- neoplastic 7 15.55%

Benign 22 48.89%

Malignant 16 35.56%

OVERALL INCIDENCE OF LESIONS

15.55%

48.89%

35.56%

0

Non- neoplastic Lesions

Benign

Malignant

60

2. SEX INCIDENCE DISTRIBUTION THE FOLLOWING

RESULTS WERE NOTED.

Male Female Total

Non-neoplastic 4.44% 11.11% 15.55%

Benign tumor 22.22% 26.67% 48.89%%

Malignant

tumour

17.78% 17.78% 35.56%

LESION AND SEX INCIDENCE

4.44%

26.67%

15.55%

48.89%

35.56%

22.22%17.78%

11.11%

17.78%

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

Non-neoplastic Benign Malignant

MALE

FEMALE

OVERALL %

61

3. AGE INCIDENCE:

Age group No. of cases Percentage

10-16 3 6.66%

20-29 5 11.11%

30-39 9 19.98%

40-49 7 15.54%

50-59 7 15.54%

60-69 9 19.98%

70-79 5 11.11%

AGE INCIDENCE OF PAROTID LESION

6.66%

11.11%

19.98%

15.54%15.54%

19.98%

11.11%

0.00%

2.00%

4.00%

6.00%

8.00%

10.00%

12.00%

14.00%

16.00%

18.00%

20.00%

2nd deca

de

3rd d

ecade

4th d

ecade

5th d

ecade

6th d

ecade

7th d

ecade

8th d

ecade

AGE INCIDENCE OF PAROTIDLESION

62

4. FNAC

FNAC has been discussed subsequently under the respective

lesions.

5. MANAGEMENT

A. SURGICAL

Superficial parotidectomy was the most commonly performed

surgery. Total conservative parotidectomy was the second most common.

TYPE OF SURGERY NO. OF CASES PERCENTAGE

SUPERFICIAL

PAROTIDECTOMY

25 55.55%

TOTAL

PAROTIDECTOMY

6 13.33%

RADICAL

PAROTIDECTOMY

1 2.22%

EXTENDED RADICAL

PAROTIDECTOMY

3 6.66%

INCISION &

DRAINAGE

3 6.66%

EXCISION 1 2.22%

COMPLETION

PAROTIDECTOMY

2 4.44%

63

B. NON-SURGICAL MODALITIES

MODALITY

RADIOTHERAPY CHEMOTHERAPY

POST

OPERATIVE PALLIATIVE

NO. OF

CASES

10 4 1

6. POST-OPERATIVE COMPLICATIONS:

Complication Percentage

Facial nerve palsy 20%

Seroma 20%

Flap Necrosis 4.44%

Fistula 4.44%

Others 2.22%

Among the other complications it was seen that one patient had

vocal cord paralysis.

64

Analysis of individual groups of lesions yielded the following

results:

1. NON- NEOPLASTIC LESION:

The study of the lesions revealed the following results

LESION MALE FEMALE

Chronic Sialadenitis - 1

Abscess 1 3

Cystic lesion 1 -

Reactive adenitis - 1

INCIDENCE OF INDIVIDUAL NON-

NEOPLASTIC LESIONS 14.28%

57.14%

14.28%

14.28%

Chronic sialdenitis

Abscess

Cystic lesion

Reactive adenitis

Abscess formed a majority of the non-neoplastic group with 4 out

of 7 cases.

65

2. SEX INCIDENCE:

SEX NO. OF

CASES PERCENTAGE

OVERALL

PERCENTAGE(ALL

LESIONS)

MALE 2 28.57% 4.44%

FEMALE 5 71.43% 11.11%

MALEFEMALE

28.57%

71.43%

0.00%

20.00%

40.00%

60.00%

80.00%

SEX INCIDENCE AMONG NON-NEOPLASTIC PAROTID LESIONS

Women were more affected by non-neoplastic parotid lesions than

men having 71.43% of the lesions.

3. FNAC

In the cytological analysis it was noted that, although there was a

higher rate of lesions which were positive, the true positives were lesser.

66

Lesion Positive FNAC Accuracy

Chronic sialadenitis 2 50%

Abscess 5 100%

Cystic lesion 2 50%

Reactive adenitis 1 100%

On further evaluvation of 3 lesions, they turned out to be Non-

Hodgkin’s lymphoma, mucoepidermoid carcinoma and pleomorphic

adenoma. Hence the overall accuracy of FNAC is around 70%.

In the data set of our study, it was found to be highly sensitive and

highly specific.

Positive predictive value of the 77% was found with this data set.

4. Age incidence:

Age group No. of patients Percentage

10-19 2 28.57%

20-29 1 14.29%

30-39 1 14.29%

40-49 2 28.57%

50-59 1 14.29%

67

AGE INCIDENCE FOR NON NEOPLASTIC LESION

28.57%

14.29%

14.29%

14.29%

28.57%

0.00% 5.00% 10.00

%

15.00

%

20.00

%

25.00

%

30.00

%

2nd decade

3rd decade

4th decade

5th decade

6th decade

5. Presentation:

Presentation No. of patients Percentage

Painful swelling 1 14.29%

Painless swelling 6 85.71

Discharge Nil -

Facial nerve palsy Nil -

Node enlargement Nil -

68

6. Treatment:

TREATMENT PERCENTAGE OVERALL

PERCENTAGE

Incision and drainage 42.86% 6.66%

Superficial parotidectomy 57.14% 8.88%

incision

and

drainag

e

superfic

ial

parotid

ectomy

0

0.1

0.2

0.3

0.4

0.5

0.6

SURGICAL MANAGEMENT OF NON-NEOPLASTIC LESIONS

incision and drainage

superficial parotidectomy

7. Complications:

Significant complications noted in this was seen only in one case

where seroma and parotid fistula developed. These resolved on its own

with time and conservative medical management.

69

7. NEOPLASTIC LESIONS:

A. BENIGN LESIONS:

It was seen that among the benign lesions, pleomorphic adenoma

was a dominant lesion. A total of 22 benign neoplasms were present in

the study which comprised of 48.88% of all lesions in the study.

1. Lesion incidence:

Lesion No. of cases Percentage Overall

percentage

Pleomorphic adenoma 20 90.9% 44.44%

Warthin’s tumor 1 4.55% 2.22%

Lipoma 1 4.55% 2.22%

INCIDENCES OF INDIVIDUAL BENIGN TUMOURS

Plem

orphic

a...

Warth

in's

tum

or

Lipom

a

BENIGN PAROTID

LESIONS

44.44%

2.22% 2.22%

90.90%

4.55% 4.55%

0.00%20.00%40.00%60.00%80.00%

100.00%

BENIGN PAROTID LESIONS

OVERALL PERCENTAGE

70

2. Sex incidence:

Sex No. of cases Percentage

Overall

percentage

Male 10 45.45% 22.22%

Female 12 54.55% 26.66%

In this category it was seen that though the incidence was

marginally more among females, males too were maximum affected by

benign lesions.

SEX INCIDENCE AMONG BENIGN LESIONS0

45.45%

54.55%

0

MALE

FEMALES

71

3. AGE INCIDENCE:

AGE

GROUP(years)

NO. OF

PATIENTS

PERCENTAGE

%

OVERALL

PERCENTAGE

(%)

10-19 1 4.54% 2.22%

20-29 2 9.09% 4.44%

30-39 6 27.27% 13.33%

40-49 4 18.16% 8.88%

50-59 4 18.16% 8.88%

60-69 4 18.16% 8.88%

70-79 1 4.54% 2.22%

Therefore the age group most susceptible to benign tumours is in

the 4th

decade. The youngest patient seen was a 16 year old male with a

lipoma.

AGE INCIDENCE FOR BENIGN TUMOURS

4.54%2.22%

9.09%

4.44%

27.27%

13.33%

18.16%

8.88%

18.16%

8.88%

18.16%

8.88%

4.54%2.22%

0.00%

5.00%

10.00%

15.00%

20.00%

25.00%

30.00%

2nd

decade

3rd

decade

4th

decade

5th

decade

6th

decade

7th

decade

PERCENTAGE

OVERALL PERCENTAGE

72

4. PRESENTATION:

Presentation No. of cases Percentage

Swelling without pain 21 46.66%

Swelling with pain 1 2.22%

Facial nerve palsy Nil

Discharge Nil

Deep lobe

involvement

Nil

Recurrence 3 6.66%

5. FNAC

Lesion Total no. detected

Pleomorphic adenoma 19

Warthin’s tumor 1

Lipoma 1

In one patient it the FNAC showed a cystic aspirate when it was

actually a pleomorphic adenoma, therefore making the total number of

pleomorphic adenoma to 20.

Sensitivity: = 100%

Specificity = 86.67%

Positive predictive value = 93.75%

Negative predictive value = 100%

73

6. TREATMENT:

Surgery was the mainstay treatment of the benign lesions. Most

underwent superficial parotidectomy barring the case of lipoma who

underwent excision of the lesion alone.

Surgery No. of cases

Percentage

overall Percentage

Superficial

parotidectomy

21 46.67 95.45

Excision 1 2.22 4.55

SURGERY FOR BENIGN PAROTID

TUMOURS0

95.45%

4.55%

Superficial parotidectomy

Excision

74

7. POST- OPERATIVE COMPLICATIONS:

Complication

No. of

patients

Percentage of

cases

Seroma 4 18.18%

Facial nerve palsy 1 4.54%

Parotid fistula 1 4.54%

POST OP COMPLICATIONS

18.18%

4.54%

4.54%

72.74%

SEROMA

FACIAL NERVE PALSY

PAROTID FISTULA

NIL

75

MALIGNANT LESIONS:

A total of 17 cases of malignant parotid tumors were there in our

study, of which the predominant type seen was mucoepidermoid

carcinoma comprising of 7 cases.

1. Incidence

Lesion No. of

cases Percentage

OVERALL % OF

INCIDENCE

Mucoepidermoid

carcinoma- low grade

4 23.54% 8.89%

Mucoepidermoid

carcinoma- high grade

3 17.66% 6.67%

Acinic cell carcinoma 1 5.88% 2.22%

Adenoid cystic

carcinoma

2 11.76% 4.44%

Carcinoma ex

pleomorphic adenoma

2 11.76% 4.44%

Undifferentiated 1 5.88% 2.22%

Lymphoma(NHL) 1 5.88% 2.22%

Adenocarcinoma 2 11.76% 4.44%

76

INCIDENCE AMONGST MALIGNANT

LESIONS

23.54%

17.66%

5.88%11.76%

11.76%

5.88%

5.88%

11.76%MUCOEPIDERMOID CA-LOWGRADEMUCOEPIDERMOID CA-HIGHGRADEACINIC CELL CA

ADENOID CYSTIC CA

CA.PLEOMORHIC ADENOMA

UNDIFFERENTIATED

LYMPHOMA

ADENOCARCINOMA

OVERALL INCIDENCE:

8.89% 6.67%

2.22%

4.44% 4.44%

2.22%

0.00%

2.00%

4.00%

6.00%

8.00%

10.00%

MUCOEPID

ERMOID

CA- L

OW G

RADE

MUCOEPID

ERMOID

CA-H

IGH G

RADE

ACINIC

CELL

CA

ADENOID C

YSTIC

CA

CA.PLE

OMORPHIC

ADENOM

A

UNDIFFE

RENTIATED

77

1. SEX INCIDENCE:

Sex No. of

cases Percentage

Overall

percentage

Male 8 50% 17.78%

Female 8 50% 17.78%

It was seen that the malignancies of the parotid affected men and

women with equal incidence.

SEX INCIDENCE

78

1. AGE INCIDENCE:

AGE(years) NO. OF

CASES PERCENTAGE

OVERALL

PERCENTAGE

10-19 NIL

20-29 2 12.5% 4.44%

30-39 2 12.5% 4.44%

40-49 1 6.25% 2.22%

50-59 2 12.5% 4.44%

60-69 5 31.25% 11.1%

70-79 4 25% 8.88%

The maximum incidence of malignancies was noted too be in the

7th

decade seen in 31.25% of malignancies closely followed by the 8th

decade affected in 25%.

79

AGE INCIDENCE FOR MALIGNANT TUMOURS

12.50%

4.44%

12.50%

4.44%6.25%

2.22%

12.50%

4.44%

31.25%

11.10%

25%

8.88%

0.00%

5.00%

10.00%

15.00%

20.00%

25.00%

30.00%

35.00%

3rd

decade

4th

decade

5th

decade

6th

decade

7th

decade

8th

decade

Age incidence of malignantparotid tumors

Overall incidence

4. Presentation

Presentation No. of cases Percentage Overall

percentage

Swelling with

pain

4 25% 8.88%

Painless swelling 12 75% 26.67%

Facial nerve

palsy

6 37.5% 13.33%

Nodes 8 50% 17.78%

Skin 4 25% 8.89%

Deep lobe

involvement

2 12.5% 4.44%

Discharge 1 6.25 2.22%

Recurrence 6 37.5% 13.33%

Mobility

restricted

5 31.25% 11.11%

80

It was noted that half the cases of malignant parotid tumours

presented with enlarged cervical nodes and a significant number of cases

(37.5%) had associated facial nerve palsy.

AGE INCIDENCE FOR MALIGNANT PAROTID TUMOURS

25%

75%

37.50%

50%

25%

12.50%

37.50%31.25%

6.25%

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

Swellin

g with

pain

Painle

ss sw

elling

Facia

l nerv

e pal

sy

NodesSk

in

Deep lobe in

volve

ment

Discharg

e

Recurre

nce

Mobilit

y rest

ricte

d

Percentage

Overall percentage

FNAC

LESION Total no. Of

positives

Mucoepidermoid carcinoma 6

Acinic cell carcinoma 3

Adenoid cystic carcinoma nil

Adenocarcinoma nil

Carcinoma pleomorphic adenoma 2

Malignant cells 3

81

With FNAC it was seen that 14 malignant tumors were detected.

The final histopathology report showed that a total of 16 malignant

parotid lesions were present.

It was seen that there were several errors in the detection of

malignant lesions, not only regarding the type of lesion that was detected

but in fact many were concluding a wrong result

Sensitivity = 87.5%

Specificity = 100%

Positive predictive value = 100%

Negative predictive value = 93.55%

2. TREATMENT MODALITIES:

Surgical modality was the mainstay treatment for most cases and

the most commonly performed surgery was total parotidectomy, it

comprised around 37.5%. Also neck dissection was performed in 31.5%

of the cases.

82

Surgery No. of cases Percentage Overall

percentage

Total conservative

parotidectomy

6 37.5% 13.33%

Radical

parotidectomy(including

extended radical

parotidectomy)

4 25% 8.89%

Completion

parotidectomy

2 12.5% 4.44%

Neck dissection 5 31.25% 11.11%

Non-surgical

management

4 25% 8.89%

Other modalities

Radiotherapy was used in almost all cases, either in the form of

palliation or post-operatively as an adjuvant. Adjuvant radiotherapy was

given in 62.5% of the cases of malignancies and as palliation in 31.25%

of cases. Chemotherapy was given as an adjuvant in one case where the

diagnosis was Non-Hodgkin’s lymphoma (CHOP Regimen) and as

palliation 1 case.

83

TREATMENT OF PAROTID MALIGNACIES

37.50%

25%12.50%

25%

25% TOTAL PAROTIDECTOMY

RADICAL PAROTIDECTOMY

COMPLETIONPAROTIDECTOMY

NON-SURGICAL

NECK DISSECTION

3. POST-OPERATIVE COMPLICATIONS:

The most common post-operative complication noted in this group

of patients was facial palsy due to injury to the facial nerve, seen in 50%

of the cases. Also seroma formation was noted in 31.25% of the patients

who underwent surgery. One patient had vocal cord palsy, due to the

extensive dissection and resection of the infiltrative tumour.

COMPLICATION NO. OF

CASES PERCENTAGE

OVERALL

PERCENTAGE

VII nerve palsy 8 50% 17.78%

Seroma 5 31.25% 11.11%

Flap necrosis 2 12.5% 4.44%

Vocal cord palsy 1 6.25% 2.22%

84

POST-OPERATIVE COMPLICATIONS FOR MALIGNANT

TUMOURS

50%

31.25%

12.50%

6.25%

17.78%

11.11%

4.44% 2.22%

0

0.1

0.2

0.3

0.4

0.5

0.6

VII nerve

palsy

Seroma Flap

necrosis

Vocal cord

palsy

PERCENTAGE AMONGMALIGNANT TUMORS

OVERALL PERCENTAGE

85

DISCUSSION

The comparative analysis of the study was made with other

published studies and the following results were obtained.

1. COMPARISON OF SEX INCIDENCE BETWEEN OUR

INSTITUTION AND VARIOUS CENTRES:

Institution KMC

M D Anderson

cancer center8

Shaw Tsai et

al6

Male:female 1:1.25 1.02: 1 1.03:1

Male 20 77 53

Female 25 75 55

1

1.25

1.02 11.03 1

0

0.2

0.4

0.6

0.8

1

1.2

1.4

Male Female

KMCH

M D Anderson

Shaw Tsai et al

Our centre showed a slightly higher incidence among females in

comparison to other centres.

86

1. FNAC COMPARISON BETWEEN OUR INSTITUTION AND

VARIOUS CENTRES

CENTRE KMC

M D ANDERSON

CANCER CENTRE8

Italy, picconi

et al14

SPECIFICITY 93.75% 86% 99%

SENSITIVITY 93.33% 82% 81%

PPV 96.87% 85% 93%

NPV 96.77% 86% 98%

FNAC COMPARISON AMONG VARIOUS CENTRES

86%82%

99%

81%

93.75%

93.33%

0.00%

20.00%

40.00%

60.00%

80.00%

100.00%

120.00%

SENSITIVITY SPECIFICITY

KMC

MD ANDERSONCANCER CENTRE

L.O.PICCONI et al

87

2. Incidence of various lesions among institutes:

Centre

NON-

NEOPLASTI

C LESIONS

BENIGN

TUMORS

MALIGNANT

TUMORS

KMCH 15.55% 48.89% 35.56%

M D ANDERSON8 7.14% 43.51% 49.35%

Shaw Tsai et al6 13.89% 77.81% 8.3%

15.55%

7.14%

13.89%

48.89%

43.51%

77.81%

35.56%

49.35%

8.30%

0.00% 20.00

%

40.00

%

60.00

%

80.00

%

100.00

%

120.00

%

KMCH

M D ANDERSON

SHAW TSAI et al

NON-NEOPLASTIC LESION

BENIGN TUMOR

MALIGNANT TUMOR

It was seen that among all the centers results for most common

benign and malignant lesions were corresponding with each other, with

pleomorphic adenoma and mucoepidermoid carcinoma respectively.

88

LESION BENIGN LESION MALIGNANT TUMOR

KMCH PLEOMORPHIC

ADENOMA (44.44%)

MUCOEPIDERMOID

CARCINOMA (6.67%)

MD

ANDERSON8

PLEOMORPHIC

ADENOMA (24.68%)

MUCOEPIDERMOID

CARCINOMA (5.19%)

L.O. Piccioni

et al 14

PLEOMORPHIC

ADENOMA(57.85%)

MUCOEPIDERMOID

CARCINOMA(2.85%)

INCIDENCE OF PLEOMORPHIC ADENOMA AND MUCO-

EPIDERMOID CARCINOMA AMONG THE INSTITUTES

KMCH

M D

ANDERSO

N

L.O P

ICCIP

NI et a

l

PLEOMORPHIC

ADENOMA

0.00%10.00%20.00%30.00%40.00%50.00%60.00%

PLEOMORPHIC ADENOMA

MUCOEPIDERMOID CARCINOMA

89

3. SURGICAL MANAGEMENT:

Superficial

parotidectomy

Total

conservative

parotidectom

y

Total

parotidetom

y with facial

nerve

resection

Radical

parotide

ctomy

Neck

dissection Others

KMCH 53.33% 13.33% 8.89% 11.11% 13.33%

Nagarkar et

al24

79.17% 12.5% 4.17% 4.17% 4.16%

Acar A, et al

25

74.4% 16.28% 6.98% - 13.95% 2.32%

In our study it was found that the other surgeries performed were

completion parotidectomy, incision drainage and excision biopsies which

corresponded with other studies.

SURGICAL MANAGEMENT AT VARIOUS CENTRES

53.33%13.33%

8.89%

79.17%12.50%

4.17%

74.40%16.28%

0.00% 20.00% 40.00% 60.00% 80.00%

KMCH

Nagarkar et

al

Acar A et al RADICAL PAROTIDECTOMY

TOTAL CONSERVATIVEPAROTIVE

SUPERFICIAL PAROTIDECTOMY

90

OTHER TREATMENT MODALITIES:

Radiotherapy was used as a postoperative adjuvant management in

most cases of malignant tumors.

POST OPERATIVE

RADIOTHERAPY

KMCH 62.5%

Acar A et al25

84.4%

Nagarkar et al24

20%

4. Postoperative complications

Most common complication of surgery was noted to be facial nerve

palsy, transient or permanent.

POSTOP

COMPLICATION

FACIAL

NERVE

PALSY

SEROMA/

HEMATOMA

FLAP

NECROSIS/

INFECTION

PAROTID

FISTULA

KMCH 20% 20% 4.44% 4.44%

Acar A et al 25

30.1% 5.8% 4.6% 3.4%

Nagarkar et al24

29.17% - - 8.33%

91

POST-OPERATIVE COMPLICATIONS AT VARIOUS CENTRES

20%

30.10%29.17%

20%

0

5.80%4.44%

3.40%

8.33%

0%

5%

10%

15%

20%

25%

30%

35%

KMCH Acar A et al Nagarkar et al

FACIAL NERVE PALSY

SEROMA/ HEMATOMA

PAROTID FISTULA

92

CONCLUSION

The analysis of the data of the study conducted at our institution

provided us with the following results:

1. Parotid lesions comprised of the most common salivary gland lesions

in our hospital.

2. Amongst the various lesions it was noted that benign tumours were

the most common and the least common were non-neoplastic

disorders.

3. The sex incidence showed a similar distribution among both males

and females with the ratio being 1:1.25.

4. The mean age of presentation was 49 yearsand it was seen that the

4th and 7th

decades where the predominant age group for occurrence

in case of benign and malignant tumours respectively.

5. The lesions which were predominant in the non-neoplastic, benign

and malignant tumours groups where abscess, pleomorphic adenoma

and mucoepidermoid carcinomas respectively. These were found to

be consistent with the comparison made with world statistics.

6. FNAC correlated in a total of 39 out of 45 cases, i.e.86.67% of the

cases.

The sensitivity and specificity for detection of benign tumors was

found to be 93.75% and 100% respectively. In the case of malignant

93

tumours the sensitivity and specificity was found to be 87.5% and 100%

respectively.

8. Patients presenting with facial nerve palsy was seen more amid the

malignant tumors.

9. Most commonly performed surgery was superficial parotidectomy.

Completion parotidectomy was performed in 2 cases and both were

malignant tumors with recurrence.

10. Facial nerve palsy and seroma formation were the commonest

complication noted post-operatively.

11. Radiotherapy was the most common non-surgical modality used

and administered more commonly post-operatively.

BIBILOGRAPHY

1. Joseph Attie et al ; in Tumors of major and minor salivary glands : clinical and

pathologic features in Chicago : Year Book Medical Publisher, 1981.Current

problems in surgery, v. 18, no. 2.

2. Anatomy of the facial nerve branching patterns, the Marginal mandibular branch

and its extra parotid Ramification in relation to the lateral palpebral line

Weerapant et al, Asian Biomedicine Vol. 4 No. 4 August 2010; 603-608

3. Davis RA, Anson BJ, Budinger JM, Kurth LR. Surgical Anatomy of the facial

nerve and parotid gland based upon a study of 350 cervicofacial halves. Surg

Gynecol Obstet. 1956; 102:385-413.

4. Facial nerve;pattern of distribution in the parotid gland; DR. FAROOQ AHMED

et al , The Professional vol:12, no:01 jan, feb, mar, 2005

5. Anatomy and physiology of the salivary glands, Grand Rounds Presentation,

UTMB, Dept. Of Otolaryngology Frederick S. Rosen, MD; Byron J. Bailey, MD

6. Parotid neoplasms: diagnosis, treatment, and intraparotid Facial nerve anatomy ;

Stella Chin-Shaw Tsai, M.D., Ph.D.*, Hsin-Te Hsu, M.D.; The Journal of

Laryngology & OtologyMay 2002, Vol. 116, pp. 359–362

7. Lundeberg D: Nonneoplastic disorders of the parotid gland West J Med 1983 Apr;

138:589-595.

8. Fine-Needle Aspiration of 154 Parotid Masses with Histologic Correlation Ten-

Year Experience at the University of Texas M. D. Anderson Cancer Center;

Basim M. Al-Khafaji, M.B., Ch.B. Blake R. Nestok, M.D. Ruth L. Katz,

M.D.Cancer (Cancer Cytopathol) 1998;84:153–9. © 1998 American Cancer

Society.

9. Tumours of the salivary glands; J.W. Eveson, P. Auclair, D.R. Gnepp, A.K. El-

Naggar; in Head and Neck tumors, Lyon; IARC Press 2005, P 209-281

10. ACS SURGERY Principles and Practice of Surgery, 6th

Edition 2007; Souba,

Wiley W

11. Review of Fine-Needle Aspiration Cytology of Salivary Gland Neoplasms, With

Emphasis on Differential Diagnosis Perkins Mukunyadzi, MD; Am J Clin Pathol

2002

12. Sonographically Guided Fine-Needle Aspiration Biopsy of Major Salivary Gland

Masses: A Review of 245 Cases Hee Woo Cho1, Jinna Kim1, Junjeong Choi2,

Hyun Seok Choi1, Eun Soo Kim1, Se-Heon Kim3 and Eun Chang Choi3

13. Mcwhorter, G. L.: Relations of Superficial and Deep Lobes of Parotid Gland to

Duct and Facial Nerve. Anat. Rec., 12:149, 1917.

14. Fine-needle aspiration cytology in the diagnosis of parotid lesions, L.O. Piccioni,

B. Fabiano, M. Gemma1, D. Sarandria, M. Bussi ACTA otorhinolaryngologica

italica 2011;31:1-4

15. Zbaren P, Schar C, Hotz MA, Loosli H. Value of fine needle aspiration cytology

of parotid gland masses. Laryngoscope 2001;111:1989-92.

16. Arshad AR. Parotid swellings: report of 110 consecutive cases. Med J Malaysia

1998;53:417-22.

17. Batsakis JG: Non-neoplastic diseases of the salivary glands, chap 3,Tumors of the

Head and Neck, 2nd Ed. Baltimore, Williams & Wilkins,1979

18. Treatment of complications of parotid gland surgery. MARCHESE-RAGONA, C.

DE FILIPPIS, G. MARIONI, A. STAFFIERI Department of Otolaryngology-

Head Neck Surgery, University of Padua, Padua, Italy; ACTA

OTORHINOLARYNGOL ITAL 25, 174-178, 2005

19. Staffieri A, Marchese Ragona R, de Filippi, s C, Tugnoli V. Management of

parotid fistulae and sialoceles with botulinum toxin. Otolaryngol Head Neck Surg

1999;121:P240-1.

20. Washington manual of surgical pathology 1st Edition, Chapter 6, Salivary Glands;

James S. Lewis Jr., Elise L. Krejci

21. Sabiston text book of surgery 18th

edition

22. Sonographically Guided Core Biopsy of A Parotid Mass : David C. Howlett Leon J. Menezes, Khari

Lewis, Andrew B. Moody, Nick Violaris, Michael D. Williams

23. Master of surgery, Joseph E Fisher, 5th

Edition, Lippincott Williams & Wilkins;

Volume I ; Head and Neck, The Parotid Gland

24. Salivary gland tumors - our experience Nitin m. Nagarkar, sandeep bansal, arjun

dass, surinder k. Singhal, harsh mohan; Indian journal of otolaryngology and head

and neck surgery vol. 56 no. 1, january - March 2004

25. Retrospective Evaluation of Parotidectomy Cases Aydın ACAR1, Adil

ERYILMAZ1, Melih ÇAYÖNÜ1, Halit AKMANSU1, Celil GÖÇER1, Bengi

ARSLAN MUTLU1, Hayriye KARABULUT; Eur J Surg Sci 2010;1(2):47-52

26. Correlation between fine needle aspiration biopsy and histologic findings in

parotid masses. Personal experience ; A.M. CONTUCCI et al, ACTA

OTORHINOLARYNGOL ITAL 2003,23:314-318

PROFORMA

NAME AGE & SEX IP No.

OCCUPATION SOCIO-ECONOMIC STATUS

ADDRESS

HISTORY

PRESENTING HISTORY:

SWELLING DURATION DISCHARGE PAIN

SYMPTOMS OF FACIAL NERVE INVOLVEMENT

OTHER

PAST:

EXPOSURE TO RADIATION TREATMENT FOR SIMILAR LESION

PERSONAL

ALCOHOL SMOKING TOBACCO/ BETEL NUT CHEWING

EXAMINATION:

GENERAL EXAMINATION :

BUILD & NUTRITION

ANAEMIA CLUBBING LYMPH NODE ENLARGEMENT

LOCAL EXAMINATION:

NUMBER SITE SIZE SHAPE SKIN SURFACE

INDURATION

WARMTH TENDERNESS CONSISTENCY MOBILITY

BI-DIGITAL PALPATION

FACIAL NERVE INVOLVEMENT

REGIONAL LYMPH NODE ENLARGEMENT

INVESTIGATIONS:

FNAC REPORT

BLOOD INVESTIGATIONS : Hb% ESR TC & DC

RADIOLOGICAL:

USG SWELLING

CT HEAD AND NECK

TREATMENT

SURGERY

OTHER MODALITY USED

POST – OPERATIVE COMPLICATIONS IF ANY AND MANGEMENT

HISTO-PATHOLOGICAL REPORT:

Name

Age &

Sex IP No. Prev Sx Side Size Past History Habits Duration

VII Nerve

Involvement Mobility

Discharg

e Skin Nodes Pain

Deep

Lobe FNAC HPE Surgery Other Findings Other Rx

P.O.

Complications

Jayaeshwari 55/F 232 no left 6x5cm nil nil 3 years nil mobile nil free

level IB,II,

III, IV,V nil nil ChSA NHL

Lt. RP +

RND muscle

infiltration

CHOP

Regimen left VC plasy

Palaniammal 38/F 289 no left 4x5cm nil

tobacco

chewing 3 months nil mobile nil free nil nil nil MEC MEC- LG Lt TCP nil nil seroma

Mahalakshmi 48/F 258 no left 3x3cm nil nil 1 year nil mobile nil free level II nil nil RA RA Lt SP nil nil nil

Karthiga 21/F 269 yes left 4x3cm

prev

swelling+ nil 6 months nil fixed nil

scar +,

skin

scarred level II nil involved ACCA AdCA

Lt

ERP+Level

II ND

facial nerve trunk

encased P.O. RT VII N

Palaniammal 60/f 303 yes right 4x5cm

parotid

abcess

drainage-

15yrs ago

tobacco

chewing 3 months nil mobile nil free nil yes involved

positive for

malignancy U.CA Lt. ERP

musccle

infiltration+,

zygomatico-

temporal P.O. RT VII N

Meenambal 75/F 52 no left 4X6cm nil

tobacco

chewing 6months nil fixed nil involved

Level

II,III,IV,V yes nil s/o malignancy Ad.CCA

Lt. TCP Lt.

RND

muscle

infiltration P.O. RT VII N

Ramasamy 62/M 652 yes right 5x7cm

prev

swelling+ smoking 8months nil mobile nil involved level II nil nil CXPA MPA Rt TCP

infiltration to

muscle, , all

margins +ve P.O. RT

seroma, flap

necrosis

Jayalakshmi 50/F 602 yes right 4x5cm

prev

swelling+ nil 1 year yes mobile nil free nil nil nil ACCA MEC- LG Rt CP

margins free,

node-reactive

hyperplasia P.O. RT

seroma, facial

palsy

Munusamy 72/M 386 no right 6x7cm nil nil 1 month yes nil yes ulceration

level IB,IA,

III nil nil

acute

supurative

inflammation MEC- LG Nil P.RT nil

Vasantha 65/F 1418 no left 7x7cm nil nil 1 1/2 years yes nil nil fixed level IB,II, yes nil MEC AdCA

Lt. ERP+

Lt. RND

muscle

infiltration,

arterial

encasement P.O. RT

Facial nerve

palsy

Ramasamy 70/M 55 no left 8x6cm nil

tobacco

chewing 1 year yes fixed nil free nil nil nil

s/o malignancy-

probably

mucoepidermo

id Ca MEC- HG nil nil P.RT nil

Citi Babu 64/M 1231 yes right 5x3cm nil nil 8months nil nil nil scar nil nil nil ACCA

cystic

neoplasm of

parotid Rt. CP nil P.O. RT nil

Guna Sundari 26/F 1327 yes right 5x2cm nil nil 7yrs nil mobile nil NIL level II nil nil MEC MEC-LG Rt TCP

lower facial

nerve trunk

involved P.O. RT

Facial nerve

palsy

Ravi 45/M 1240 no right 12x7cm nil smoking 6months nil fixed nil free nil yes nil CXPA CXPA nil P.RT

Facial nerve

palsy

Durga Devi 17/F 18419 no right 5x4cm nil nil 1week nil mobile nil NIL nil yes nil abscess Rt. I&D nil nil nil

Kanagavalli 37/F 14375 no left 6x4cm nil nil 10 days nil mobile nil nil nil yes nil abscess Rt. I&D nil nil nil

Jayalakshmi 39/F 12797 yes right 6x5cm nil nil 1 1/2 years nil mobile nil nil nil nil nil PA PA Rt. SP nil nil nil

Dhayalan 63/M 9176 no right 6x7cm nil nil 10months nil mobile nil nil nil nil nil MEC MEC-HG

Rt.

TCP+RND nil P.O. RT

seroma, flap

necrosis

Jayalakshmi 39/F 11147 no right 5x6cm nil nil 1 year yes mobile NIL NIL nil nil nil ACCA ACCA Rt TCP nil P.O. RT

seroma, facial

palsy

Arun Kumar 16/M 11952 no left 3x4cm nil nil 6months nil mobile nil NIL nil nil nil lipoma lipoma Lt. Ebx nil nil nil

Saroja 35/F 13343 no left 2x2cm nil nil 1year nil mobile nil NIL nil yes nil PA PA Lt. SP nil nil nil

Deepa 16/F 20123 no left 3x4cm nil nil 10days nil nil nil nil nil yes nil abscess Lt. I&D nil nil nil

Mosaraj Rathinam 54/M 18678 no right 5x6cm nil smoking 3 months nil mobile nil nil nil yes nil abscess

chronic

abscess Rt.SP nil nil nil

Appandu 65/M 24950 yes right 6x7cm nil nil 3 months nil mobile nil scar+ nil nil nil PA PA Rt.SP nil nil nil

Matheena Beevi 63/F 17580 no right 6x4cm nil nil 7 months nil mobile nil NIL nil nil nil PA PA Rt.SP nil nil

Facial nerve

palsy

Mohideen 50/ M 25629 no left 8x6cm nil smoking 2 years nil mobile nil nil nil nil nil WT WT Rt.SP nil nil seroma

Govindaraj 42/M 23032 no right 5x4cm nil nil 9months nil mobile nil nil nil nil nil PA PA Rt.SP nil nil nil

Rajagopal 57/M 1576 no left 6x5cm nil nil 6months nil mobile nil NIL nil nil nil PA PA Lt.SP nil nil nil

Chinnamal 55/F 1657 no left 6x4cm nil nil 1 year nil mobile nil NIL nil nil nil PA PA Lt.SP nil nil nil

Satya 35F 12697 no right 5x4cm nil nil 8 months nil mobile nil nil nil nil nil PA PA Rt.SP nil nil nil

Haridas 42/M 24561 no right 4x3cm nil nil 7 months nil mobile nil NIL nil nil nil cystic aspirate parotid cyst Rt.SP nil nil

seroma, parotid

fistula

Malliga 34/F 3568 no left 3x4cm nil nil 6 months nil mobile nil nil nil nil nil PA PA Lt.SP nil nil parotid fistula

thirunavukarasu 70/M 13321 no right 6x4cm nil nil 8 months yes fixed nil fixed

Level

II,III,IV nil nil MEC MEC-HG nil P.RT nil

Elumalai 29/M 1987 no right 3x4cm nil smoking 6 months nil mobile nil NIL nil nil nil PA PA Rt.SP nil nil nil

Velammal 60/F 15667 no left 5x6cm nil nil 1 year nil mobile nil NIL nil nil nil PA PA Lt.SP nil nil nil

Devaki 32/F 11451 no right 4x3cm nil nil 5months nil mobile nil NIL nil nil nil PA PA Rt.SP nil nil seroma

Dhanapal 49/M 12891 no right 5x3cm nil nil 7 months nil mobile nil NIL nil nil nil PA PA Rt.SP nil nil nil

Amutha 28/F 23013 no left 4x3cm nil nil 8 months nil mobile nil NIL nil nil nil PA PA Lt.SP nil nil nil

Janaki Raman 33/M 30012 no right 6x4cm nil nil 1 1/2 years nil mobile nil NIL nil nil nil PA PA Rt.SP nil nil nil

Jayanthi 47/F 23971 yes left 4x3cm nil nil 6 months nil mobile nil scar + nil nil nil PA PA Lt.SP nil nil seroma

Chellamai 52/F 1784 no left 5x4cm nil nil 9months nil mobile nil NIL nil nil nil PA PA Lt.SP nil nil nil

Kumar 41/M 16671 no right 3x4cm nil nil 6 months nil mobile nil NIL nil nil nil cystic aspirate PA Lt.SP nil nil seroma

Kamala 65/F 3224 no right 5x4cm nil

tobacco

chewing 1 year nil mobile nil NIL nil nil nil PA PA Rt.SP nil nil nil

Kodeshwari 50/F 5030 no right 4x3cm nil nil 1 1/2 years nil mobile nil NIL nil yes nil C.SA C.SA Rt.SP nil nil nil

Bahadur 77/M 3903 no right 6x5cm nil nil 1 year nil mobile nil NIL nil nil nil PA PA Rt.SP nil nil nil

KEY TO MASTER CHART

CSA - Chronic Sialadenitis

MEC - Mucoepidermoid Carcinoma

PA - Pleomorphic Adenoma

RA - Reactive adenitis

ACCA - Acinic cell tumor Carcinoma

Ad. CA - Adenoid cystic Carcinoma

UCA - Undifferentiated carcinoma

CxPA - Carcinoma ex pleomorphic adenoma

WT - Warthin’s tumour

Inf - Inflammatory

PRT - Palliative RT

PORT - Postoperative RT

RP - Radical parotidectomy

TCP - Total conservative parotidectomy

SP - Superficial parotidectomy

ERP - Extended radical parotidectomy

CP - Completion parotidectomy

I&D - Incision and drainage

RND - Radical Neck Dissection